Alzheimer's disease is a disorder associated with cognitive dysfunctions, and is characterized by a loss of nerve cells and emergence of a large number of senile plaques and neurofibrillary tangles. Senile plaques are detected at the earliest stage of development of this disease. These plaques are highly specific to this disease since they are not found in other neurodegenerative disorders. Amyloid-β protein (Aβ) is the major constituent of senile plaques and forms amyloid fibrils having a β-sheet structure. Aβ is a polypeptide comprising approximately 40 amino acid residues and has a molecular weight of 4,000 Da. It easily aggregates to form fibrils and becomes insoluble. The major molecular species of this protein are Aβ40, which ends with valine at amino acid residue 40, and Aβ42, the longer form of Aβ having two additional residues. Although Aβis usually degraded and never accumulates in the brain, the degrading capacity decreases with aging, causing an accumulation of Aβ. This triggers neuronal dysfunction and cell death, ultimately resulting in dementia and Alzheimer's disease. Through various genetic analyses and molecular biological and neuropharmacological studies, “amyloid hypothesis” has been proposed as a cause of the pathogenesis of Alzheimer's disease.